Fear is a normal reaction to danger, but when fear response are routinely expressed inappropriately, a fear or anxiety disorder exists. One of the leading ideas is that anxiety disorders reflect malfunctions in the brain system that evolved to detect danger and execute defense responses. Many of the stimuli that activate this system, the fear system, in humans are not hard-wired into the brain s circuitry, but instead are learned about through experience. The proposed research is thus aimed at understanding how the brain learns and stores information about danger. Classical fear conditioning is used as a behavioral procedure through which an innocuous stimulus (a conditioned stimulus) when associated with an aversive event (an unconditioned stimulus), acquires the capacity to elicit fear reactions. The hypothesis being tested is that the amygdala plays an essential role in the plasticity that underlies fear conditioning. This hypothesis is supported by considerable evidence, but some fundamental questions concerning its validity remain unanswered. The aims of this proposal are to clarify issues concerning the neural pathways which an acoustic conditioned stimulus is transmitted to the amygdala, the patterns of information flow within the amygdala, the necessity of the amygdala for the acquisition and storage process, and the nature of neural coding in various components of the circuitry. Together, these studies represent an integrated, multidisciplinary research program aimed at understanding the nature of fear and will hopefully provide information that will be useful in preventing or treating disorders.